The precise mechanisms by which ACLY inhibition increases CXCL13 and TLS formation remain undefined; however, future studies investigating whether reductions in the levels of tumour metabolites such as fatty acids and succinate or increase in the levels of citrate directly impact tumoural B cell recruitment and formation of TLSs or, alternatively, whether there are reductions in the level of CXCL13 promoter acetylation will be important. Here, CXCL13 is linked to neoplasm.